Glomerulonephritis (GN) generally refers to a kidney tissue lesion which manifests with the appearance of immunoreaction or inflammatory response in the glomerulus. Generally, it is not caused by a direct infection of the glomerulus itself, but some induced inflammatory response caused by the immune complex induced by the infection in other parts of the body or autoimmune disease which deposits in the glomerulus through blood circulation which results in the damage of the glomerulus. Glomerulonephritis is one of the main causes of chronic kidney disease (CDK). If not treated in time, it is likely to develop into chronic renal failure, which ultimately will result in the loss of function of the kidney and entering of the end-stage renal disease.
The characteristics of clinical manifestation of glomerulonephritis are mainly hematuria and proteinuria. In addition, macrophage infiltration in the kidney tissue is generally observed. Relative research believes that macrophages express many pro-inflammation cytokines and chemokines such as TNF-α, IL-1β, IL-6, IL-18, IL-23, MIP-1, MIP-2 and MCP-1 etc., which are simultaneously involved in oxidative stress response. Moreover, activated macrophages secrete matrix metallopeptidase 9 (MMP9), which leads to the transformation of epithelial cells to mesenchymal cells, causing sclerosis of the kidney tissue. Currently there are researches focusing on macrophage to develop treatment for glomerulonephritis, such as using drugs or vaccine to disrupt the accumulation of macrophages in the kidney, or even using gene modification to reduce macrophage activity to reduce the damage in the kidney.
Generally, immunosuppressors such as steroid or cyclosporine have been used for the treatment of glomerulonephritis, but they often cause severe side effects. In recent years, angiotensin converting enzyme inhibitor (ACEi) or angiotensin receptorblocker (ARB) are also used for the treatment to delay the progression of the kidney disease. However, some reports have indicated that long-term use of such drugs can possibly cause progression of kidney dysfunction, particularly in patients with renal arterial stenosis.
Cinammomum osmophloeum Kaneh is an evergreen woody plant that is epidemic to Taiwan, which its branches, leaves and bark are enriched with essential oil. The extracted oil has similar ingredients as cinnamon oil, being mainly cinnamalydehyde (80%), salicylic acid and eugenol, wherein cinnamalydehyde has been proven to have many curative effects such as anti-tumor (Cancer Lett, 196: 143-152, 2003), anti-inflammation (Food Chem Toxicol, 46: 220-231, 2008; Eur J Pharmacol, 537: 174-180, 2006; Biochem Pharmacol, 75: 494-502, 2008; Mediators Inflamm, 2010: 529359, 2010), anti-bacteria (Toxicol Appl Pharmacol, 244: 174-180, 2010), anti-oxidation (Cancer Lett, 196: 143-152, 2003; Biochem Pharmacol, 69: 791-799, 2005.) and can regulate blood glucose and blood lipid through regulating the activity of saccharide transport proteins and modifying insulin's functions (Food Chem Toxicol, 48: 2344-2349, 2010; Phytomedicine, 14: 15-22, 2007; Biochimie, 93: 339-344, 2010.), while it can also regulate platelet agglutination and lower the amount of uric acid in urine (Toxicol Appl Pharmacol, 244: 174-180, 2010). Previous studies also showed that cinnamaldehyde has a certain level of cytotoxicity to cells. Until today, no literatures have reported a cinnamaldehyde derivative having renoprotective effects in treating or ameliorating symptoms of glomerulonephritis.